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Race should no longer be used to describe populations in most genetics studies, a panel of experts says.

Using race and ethnicity to describe study participants gives the mistaken impression that humans can be divided into distinct groups. Such labels have been used to stigmatize groups of people, but do not explain biological and genetic diversity, the panel convened by the U.S. National Academies of Sciences, Engineering and Medicine said in a report on March 14.
In particular, the term Caucasian should no longer be used, the committee recommends. The term, coined in the 18th century by German scientist Johann Friedrich Blumenbach to describe what he determined was the most beautiful skull in his collection, carries the false notion of white superiority, the panel says.

Worse, the moniker “has also acquired today the connotation of being an objective scientific term, and that’s what really led the committee to take objection with it,” says Ann Morning, a sociologist at New York University and a member of the committee that wrote the report. “It tends to reinforce this erroneous belief that racial categories are somehow objective and natural characterizations of human biological difference. We felt that it was a term that … should go into the dustbin of history.”

Similarly, the term “black race” shouldn’t be used because it implies that Black people are a distinct group, or race, that can be objectively defined, the panel says.

Racial definitions are problematic “because not only are they stigmatizing, they are historically wrong,” says Ambroise Wonkam, a medical geneticist at Johns Hopkins University and president of the African Society of Human Genetics. Race is often used as a proxy for genetic diversity. But “race cannot be used to capture diversity at all. Race doesn’t exist. There is only one race, the human race,” says Wonkam, who was not involved with the National Academies’ panel.

Race might be used in some studies to determine how genetic and social factors contribute to health disparities (SN: 4/5/22), but beyond that race has no real value in genetic research, Wonkam adds.

Researchers could use other identifiers, including geographical ancestry, to define groups of people in the study, Wonkam says. But those definitions need to be precise.

For instance, some researchers group Africans by language groups. But a Bantu-speaking person from Tanzania or Nigeria where malaria is endemic would have a much higher genetic risk of sickle cell disease than a Bantu-speaking person whose ancestors are from South Africa, where malaria has not existed for at least 1,000 years. (Changes in genes that make hemoglobin can protect against malaria (SN: 5/2/11), but cause life-threatening sickle cell disease.)
Genetic studies also have to account for movements of people and mixture between multiple groups, Wonkam says. And labeling must be consistent for all groups in the study, he says. Current studies sometimes compare continent-wide racial groups, such as Asian, with national groups, such as French or Finnish, and ethnic groups, such as Hispanic.

An argument for keeping race in rare cases
Removing race as a descriptor may be helpful for some groups, such as people of African descent, says Joseph Yracheta, a health disparities researcher and the executive director of the Native BioData Consortium, headquartered on the Cheyenne River Sioux reservation in South Dakota. “I understand why they want to get rid of race science for themselves, because in their case it’s been used to deny them services,” he says.

But Native Americans’ story is different, says Yracheta, who was not part of the panel. Native Americans’ unique evolutionary history have made them a valuable resource for genetics research. A small starting population and many thousands of years of isolation from humans outside the Americas have given Native Americans and Indigenous people in Polynesia and Australia some genetic features that may make it easier for researchers to find variants that contribute to health or disease, he says. “We’re the Rosetta stone for the rest of the planet.”

Native Americans “need to be protected, because not only are our numbers small, but we keep having things taken away from us since 1492. We don’t want this to be another casualty of colonialism.” Removing the label of Indigenous or Native American may erode tribal sovereignty and control over genetic data, he says.

The panel does recommend that genetic researchers should clearly state why they used a particular descriptor and should involve study populations in making decisions about which labels to use.

That community input is essential, Yracheta says. The recommendations have no legal or regulatory weight. So he worries that this lack of teeth may allow researchers to ignore the wishes of study participants without fear of penalty.

Still seeking diversity in research participants
Genetics research has suffered from a lack of diversity of participants (SN: 3/4/21). To counteract the disparities, U.S. government regulations require researchers funded by the National Institutes of Health to collect data on the race and ethnicity of study participants. But because those racial categories are too broad and don’t consider the social and environmental conditions that may affect health, the labels are not helpful in most genetic analyses, the panel concluded.

Removing racial labels won’t hamper diversity efforts, as researchers will still seek out people from different backgrounds to participate in studies, says Brendan Lee, who is president of the American Society of Human Genetics. But taking race out of the equation should encourage researchers to think more carefully about the type of data they are collecting and how it might be used to support or refute racism, says Lee, a medical geneticist at Baylor College of Medicine in Houston, who was not part of the panel.

The report offers decision-making tools for determining what descriptors are appropriate for particular types of studies. But “while it is a framework, it is not a recipe where in every study we do A, B and C,” Lee says.

Researchers probably won’t instantly adopt the new practices, Lee says. “It is a process that will take time. I don’t think it is something we can expect in one week or one evening that we’ll all change over to this, but it is a very important first step.”

Just a few powerful storms in Antarctica can have an outsized effect on how much snow parts of the southernmost continent get. Those ephemeral storms, preserved in ice cores, might give a skewed view of how quickly the continent’s ice sheet has grown or shrunk over time.

Relatively rare extreme precipitation events are responsible for more than 40 percent of the total annual snowfall across most of the continent — and in some places, as much as 60 percent, researchers report March 22 in Geophysical Research Letters.
Climatologist John Turner of the British Antarctic Survey in Cambridge and his colleagues used regional climate simulations to estimate daily precipitation across the continent from 1979 to 2016. Then, the team zoomed in on 10 locations — representing different climates from the dry interior desert to the often snowy coasts and the open ocean — to determine regional differences in snowfall.

While snowfall amounts vary greatly by location, extreme events packed the biggest wallop along Antarctica’s coasts, especially on the floating ice shelves, the researchers found. For instance, the Amery ice shelf in East Antarctica gets roughly half of its annual precipitation — which typically totals about half a meter of snow — in just 10 days, on average. In 1994, the ice shelf got 44 percent of its entire annual precipitation on a single day in September.

Ice cores aren’t just a window into the past; they are also used to predict the continent’s future in a warming world. So characterizing these coastal regions is crucial for understanding Antarctica’s ice sheet — and its potential future contribution to sea level rise.
Editor’s note: This story was updated April 5, 2019, to correct that the results were reported March 22 (not March 25).

We live in a sea of neutrinos. Every second, trillions of them pass through our bodies. They come from the sun, nuclear reactors, collisions of cosmic rays hitting Earth’s atmosphere, even the Big Bang. Among fundamental particles, only photons are more numerous. Yet because neutrinos barely interact with matter, they are notoriously difficult to detect.

The existence of the neutrino was first proposed in the 1930s and then verified in the 1950s (SN: 2/13/54). Decades later, much about the neutrino — named in part because it has no electric charge — remains a mystery, including how many varieties of neutrinos exist, how much mass they have, where that mass comes from and whether they have any magnetic properties.
These mysteries are at the heart of Ghost Particle by physicist Alan Chodos and science journalist James Riordon. The book is an informative, easy-to-follow introduction to the perplexing particle. Chodos and Riordon guide readers through how the neutrino was discovered, what we know — and don’t know — about it, and the ongoing and future experiments that (fingers crossed) will provide the answers.

It’s not just neutrino physicists who await those answers. Neutrinos, Riordon says, “are incredibly important both for understanding the universe and our existence in it.” Unmasking the neutrino could be key to unlocking the nature of dark matter, for instance. Or it could clear up the universe’s matter conundrum: The Big Bang should have produced equal amounts of matter and antimatter, the oppositely charged counterparts of electrons, protons and so on. When matter and antimatter come into contact, they annihilate each other. So in theory, the universe today should be empty — yet it’s not (SN: 9/22/22). It’s filled with matter and, for some reason, very little antimatter.

Science News spoke with Riordon, a frequent contributor to the magazine, about these puzzles and how neutrinos could act as a tool to observe the cosmos or even see into our own planet. The following conversation has been edited for length and clarity.

SN: In the first chapter, you list eight unanswered questions about neutrinos. Which is the most pressing to answer?

Riordon: Whether they’re their own antiparticles is probably one of the grandest. The proposal that neutrinos are their own antiparticles is an elegant solution to all sorts of problems, including the existence of this residue of matter we live in. Another one is figuring out how neutrinos fit in the standard model [of particle physics]. It’s one of the most successful theories there is, but it can’t explain the fact that neutrinos have mass.
SN: Why is now a good time to write a book about neutrinos?

Riordon: All of these questions about neutrinos are sort of coming to a head right now — the hints that neutrinos may be their own antiparticles, the issues of neutrinos not quite fitting the standard model, whether there are sterile neutrinos [a hypothetical neutrino that is a candidate for dark matter]. In the next few years, a decade or so, there will be a lot of experiments that will [help answer these questions,] and the resolution either way will be exciting.

SN: Neutrinos could also be used to help scientists observe a range of phenomena. What are some of the most interesting questions neutrinos could help with?

Riordon: There are some observations that simply have to be done with neutrinos, that there are no other technological alternatives for. There’s a problem with using light-based telescopes to look back in history. We have this really amazing James Webb Space Telescope that can see really far back in history. But at some point, when you go far enough back, the universe is basically opaque to light; you can’t see into it. Once we narrow down how to detect and how to measure the cosmic neutrino background [neutrinos that formed less than a second after the Big Bang], it will be a way to look back at the very beginning. Other than with gravitational waves, you can’t see back that far with anything else. So it’ll give us sort of a telescope back to the beginning of the universe.

The other thing is, when a supernova happens, all kinds of really cool stuff happens inside, and you can see it with neutrinos because neutrinos come out immediately in a burst. We call it the “cosmic neutrino bomb,” but you can track the supernova as it’s going along. With light, it takes a while for it to get out [of the stellar explosion]. We’re due for a [nearby] supernova. We haven’t had one since 1987. It was the last visible supernova in the sky and was a boon for research. Now that we have neutrino detectors around the world, this next one is going to be even better [for research], even more exciting.

And if we develop better instrumentation, we could use neutrinos to understand what’s going on in the center of the Earth. There’s no other way that you could probe the center of the Earth. We use seismic waves, but the resolution is really low. So we could resolve a lot of questions about what the planet is made of with neutrinos.

SN: Do you have a favorite “character” in the story of neutrinos?

Riordon: I’m certainly very fond of my grandfather Clyde Cowan [he and Frederick Reines were the first physicists to detect neutrinos]. But Reines is a riveting character. He was poetic. He was a singer. He really was this creative force. I mentioned [in the book] that they put this “SNEWS” sign on their detector for “supernova early warning system,” which sort of echoed the ballistic missile early warning systems at the time [during the Cold War]. That’s so ripe.

When you’re stressed and anxious, you might feel your heart race. Is your heart racing because you’re afraid? Or does your speeding heart itself contribute to your anxiety? Both could be true, a new study in mice suggests.

By artificially increasing the heart rates of mice, scientists were able to increase anxiety-like behaviors — ones that the team then calmed by turning off a particular part of the brain. The study, published in the March 9 Nature, shows that in high-risk contexts, a racing heart could go to your head and increase anxiety. The findings could offer a new angle for studying and, potentially, treating anxiety disorders.
The idea that body sensations might contribute to emotions in the brain goes back at least to one of the founders of psychology, William James, says Karl Deisseroth, a neuroscientist at Stanford University. In James’ 1890 book The Principles of Psychology, he put forward the idea that emotion follows what the body experiences. “We feel sorry because we cry, angry because we strike, afraid because we tremble,” James wrote.

The brain certainly can sense internal body signals, a phenomenon called interoception. But whether those sensations — like a racing heart — can contribute to emotion is difficult to prove, says Anna Beyeler, a neuroscientist at the French National Institute of Health and Medical Research in Bordeaux. She studies brain circuitry related to emotion and wrote a commentary on the new study but was not involved in the research. “I’m sure a lot of people have thought of doing these experiments, but no one really had the tools,” she says.

Deisseroth has spent his career developing those tools. He is one of the scientists who developed optogenetics — a technique that uses viruses to modify the genes of specific cells to respond to bursts of light (SN: 6/18/21; SN: 1/15/10). Scientists can use the flip of a light switch to activate or suppress the activity of those cells.
In the new study, Deisseroth and his colleagues used a light attached to a tiny vest over a mouse’s genetically engineered heart to change the animal’s heart rate. When the light was off, a mouse’s heart pumped at about 600 beats per minute. But when the team turned on a light that flashed at 900 beats per minutes, the mouse’s heartbeat followed suit. “It’s a nice reasonable acceleration, [one a mouse] would encounter in a time of stress or fear,” Deisseroth explains.

When the mice felt their hearts racing, they showed anxiety-like behavior. In risky scenarios — like open areas where a little mouse might be someone’s lunch — the rodents slunk along the walls and lurked in darker corners. When pressing a lever for water that could sometimes be coupled with a mild shock, mice with normal heart rates still pressed without hesitation. But mice with racing hearts decided they’d rather go thirsty.

“Everybody was expecting that, but it’s the first time that it has been clearly demonstrated,” Beyeler says.
The researchers also scanned the animals’ brains to find areas that might be processing the increased heart rate. One of the biggest signals, Deisseroth says, came from the posterior insula (SN: 4/25/16). “The insula was interesting because it’s highly connected with interoceptive circuitry,” he explains. “When we saw that signal, [our] interest was definitely piqued.”

Using more optogenetics, the team reduced activity in the posterior insula, which decreased the mice’s anxiety-like behaviors. The animals’ hearts still raced, but they behaved more normally, spending some time in open areas of mazes and pressing levers for water without fear.
A lot of people are very excited about the work, says Wen Chen, the branch chief of basic medicine research for complementary and integrative health at the National Center for Complementary and Integrative Health in Bethesda, Md. “No matter what kind of meetings I go into, in the last two days, everybody brought up this paper,” says Chen, who wasn’t involved in the research.

The next step, Deisseroth says, is to look at other parts of the body that might affect anxiety. “We can feel it in our gut sometimes, or we can feel it in our neck or shoulders,” he says. Using optogenetics to tense a mouse’s muscles, or give them tummy butterflies, might reveal other pathways that produce fearful or anxiety-like behaviors.

Understanding the link between heart and head could eventually factor into how doctors treat panic and anxiety, Beyeler says. But the path between the lab and the clinic, she notes, is much more convoluted than that of the heart to the head.

An experimental treatment for endometriosis, a painful gynecological disease that affects some 190 million people worldwide, may one day offer new hope for easing symptoms.

Monthly antibody injections reversed telltale signs of endometriosis in monkeys, researchers report February 22 in Science Translational Medicine. The antibody targets IL-8, a molecule that whips up inflammation inside the scattered, sometimes bleeding lesions that mark the disease. After neutralizing IL-8, those hallmark lesions shrink, the team found.

The new treatment is “pretty potent,” says Philippa Saunders, a reproductive scientist at the University of Edinburgh who was not involved with work. The study’s authors haven’t reported a cure, she points out, but their antibody does seem to have an impact. “I think it’s really very promising,” she says.

Many scientists think endometriosis occurs when bits of the uterine lining — the endometrium — slough off during menstruation. Instead of exiting via the vagina, they voyage in the other direction: up through the fallopian tubes. Those bits of tissue then trespass through the body, sprouting lesions where they land. They’ll glom onto the ovaries, fallopian tubes, bladder and other spots outside of the uterus and take on a life of their own, Saunders says.
The lesions can grow nerve cells, form tough nubs of tissue and even bleed during menstrual cycles. They can also kick off chronic bouts of pelvic pain. If you have endometriosis, you can experience “pain when you urinate, pain when you defecate, pain when you have sex, pain when you move around,” Saunders says. People with the disease can also struggle with infertility and depression, she adds. “It’s really nasty.”
Once diagnosed, patients face a dearth of treatment options — there’s no cure, only therapies to alleviate symptoms. Surgery to remove lesions can help, but symptoms often come back.

The disease affects at least 10 percent of girls, women and transgender men in their reproductive years, Saunders says. And people typically suffer for years — about eight on average — before a diagnosis. “Doctors consider menstrual pelvic pain a very common thing,” says Ayako Nishimoto-Kakiuchi, a pharmacologist at Chugai Pharmaceutical Co. Ltd. in Tokyo. Endometriosis “is underestimated in the clinic,” she says. “I strongly believe that this disease has been understudied.”

Hormonal drugs that stop ovulation and menstruation can also offer relief, says Serdar Bulun, a reproductive endocrinologist at Northwestern University Feinberg School of Medicine in Chicago not involved with the new study. But those drugs come with side effects and aren’t ideal for people trying to become pregnant. “I see these patients day in and day out,” he says. “I see how much they suffer, and I feel like we are not doing enough.”

Nishimoto-Kakiuchi’s team engineered an antibody that grabs onto the inflammatory factor IL-8, a protein that scientists have previously fingered as one potential culprit in the disease. The antibody acts like a garbage collector, Nishimoto-Kakiuchi says. It grabs IL-8, delivers it to the cell’s waste disposal machinery, and then heads out to snare more IL-8.

The team tested the antibody in cynomolgus monkeys that were surgically modified to have the disease. (Endometriosis rarely shows up spontaneously in these monkeys, the scientists discovered previously after screening more than 600 females.) The team treated 11 monkeys with the antibody injection once a month for six months. In these animals, lesions shriveled and the adhesive tissue that glues them to the body thinned out, too. Before this study, Nishimoto-Kakiuchi says, the team didn’t think such signs of endometriosis were reversible.
Her company has now started a Phase I clinical trial to test the safety of therapy in humans. The treatment is one of several endometriosis therapies scientists are testing (SN: 7/19/19) . Other trials will test new hormonal drugs, robot-assisted surgery and behavioral interventions.

Doctors need new options to help people with the disease, Saunders says. “There’s a huge unmet clinical need.”

For generations of dogs, home is the radioactive remains of the Chernobyl Nuclear Power Plant.

In the first genetic analysis of these animals, scientists have discovered that dogs living in the power plant industrial area are genetically distinct from dogs living farther away.

Though the team could distinguish between dog populations, the researchers did not pinpoint radiation as the reason for any genetic differences. But future studies that build on the findings, reported March 3 in Science Advances, may help uncover how radioactive environments leave their mark on animal genomes.
That could have implications for other nuclear disasters and even human space travel, says Timothy Mousseau, an evolutionary ecologist at the University of South Carolina in Columbia. “We have high hopes that what we learn from these dogs … will be of use for understanding human exposures in the future,” he says.

Since his first trip in 1999, Mousseau has stopped counting how many times he’s been to Chernobyl. “I lost track after we hit about 50 visits.”

He first encountered Chernobyl’s semi-feral dogs in 2017, on a trip with the Clean Futures Fund+, an organization that provides veterinary care to the animals. Not much is known about how local dogs survived after the nuclear accident. In 1986, an explosion at one of the power plant’s reactors kicked off a disaster that lofted vast amounts of radioactive isotopes into the air. Contamination from the plant’s radioactive cloud largely settled nearby, in a region now called the Chernobyl Exclusion Zone.

Dogs have lived in the area since the disaster, fed by Chernobyl cleanup workers and tourists. Some 250 strays were living in and around the power plant, among spent fuel-processing facilities and in the shadow of the ruined reactor. Hundreds more roam farther out in the exclusion zone, an area about the size of Yosemite National Park.
During Mousseau’s visits, his team collected blood samples from these dogs for DNA analysis, which let the researchers map out the dogs’ complex family structures. “We know who’s related to who,” says Elaine Ostrander, a geneticist at the National Human Genome Research Institute in Bethesda, Md. “We know their heritage.”

The canine packs are not just a hodgepodge of wild feral dogs, she says. “There are actually families of dogs breeding, living, existing in the power plant,” she says. “Who would have imagined?”

Dogs within the exclusion zone share ancestry with German shepherds and other shepherd breeds, like many other free-breeding dogs from Eastern Europe, the team reports. And though their work revealed that dogs in the power plant area look genetically different from dogs in Chernobyl City, about 15 kilometers away, the team does not know whether radiation caused these differences or not, Ostrander says. The dogs may be genetically distinct simply because they’re living in a relatively isolated area.

The new finding is not so surprising, says Jim Smith, an environmental scientist at the University of Portsmouth in England. He was not part of the new study but has worked in this field for decades. He’s concerned that people might assume “that the radiation has something to do with it,” he says. But “there’s no evidence of that.”

Scientists have been trying to pin down how radiation exposure at Chernobyl has affected wildlife for decades (SN: 5/2/14). “We’ve been looking at the consequences for birds and rodents and bacteria and plants,” Mousseau says. His team has found animals with elevated mutation rates, shortened life spans and early-onset cataracts.

It’s not easy to tease out the effects of low-dose radiation among other factors, Smith says. “[These studies] are so hard … there’s lots of other stuff going in the natural environment.” What’s more, animals can reap some benefits when humans leave contaminated zones, he says.

How, or if, radiation damage is piling up in dogs’ genomes is something the team is looking into now, Ostrander says. Knowing the dogs’ genetic backgrounds will make it easier to spot any radiation red flags, says Bridgett vonHoldt, an evolutionary geneticist at Princeton University, who was not involved in the work.

“I feel like it’s a cliffhanger,” she says. “I want to know more.”

SpaceX’s rapidly growing fleet of Starlink internet satellites now make up half of all active satellites in Earth orbit.

On February 27, the aerospace company launched 21 new satellites to join its broadband internet Starlink fleet. That brought the total number of active Starlink satellites to 3,660, or about 50 percent of the nearly 7,300 active satellites in orbit, according to analysis by astronomer Jonathan McDowell using data from SpaceX and the U.S. Space Force.
“These big low-orbit internet constellations have come from nowhere in 2019, to dominating the space environment in 2023,” says McDowell, of the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass. “It really is a massive shift and a massive industrialization of low orbit.”

SpaceX has been launching Starlink satellites since 2019 with the goal of bringing broadband internet to remote parts of the globe. And for just as long, astronomers have been warning that the bright satellites could mess up their view of the cosmos by leaving streaks on telescope images as they glide past (SN: 3/12/20).

Even the Hubble Space Telescope, which orbits more than 500 kilometers above the Earth’s surface, is vulnerable to these satellite streaks, as well as those from other satellite constellations. From 2002 to 2021, the percentage of Hubble images affected by light from low-orbit satellites increased by about 50 percent, astronomer Sandor Kruk of the Max-Planck Institute for Extraterrestrial Physics in Garching, Germany, and colleagues report March 2 in Nature Astronomy.

The number of images partially blocked by satellites is still small, the team found, rising from nearly 3 percent of images taken between 2002 and 2005 to just over 4 percent between 2018 and 2021 for one of Hubble’s cameras. But there are already thousands more Starlink satellites now than there were in 2021.

“The fraction of [Hubble] images crossed by satellites is currently small with a negligible impact on science,” Kruk and colleagues write. “However, the number of satellites and space debris will only increase in the future.” The team predicts that by the 2030s, the probability of a satellite crossing Hubble’s field of view any time it takes an image will be between 20 and 50 percent.
The sudden jump in Starlink satellites also poses a problem for space traffic, says astronomer Samantha Lawler of the University of Regina in Canada. Starlink satellites all orbit at a similar distance from Earth, just above 500 kilometers.

“Starlink is the densest patch of space that has ever existed,” Lawler says. The satellites are constantly navigating out of each other’s way to avoid collisions (SN: 2/12/09). And it’s a popular orbital altitude — Hubble is there, and so is the International Space Station and the Chinese space station.
“If there is some kind of collision [between Starlinks], some kind of mishap, it could immediately affect human lives,” Lawler says.

SpaceX launches Starlink satellites roughly once per week — it launched 51 more on March 3. And they’re not the only company launching constellations of internet satellites. By the 2030s, there could be 100,000 satellites crowding low Earth orbit.

So far, there are no international regulations to curb the number of satellites a private company can launch or to limit which orbits they can occupy.

“The speed of commercial development is much faster than the speed of regulation change,” McDowell says. “There needs to be an overhaul of space traffic management and space regulation generally to cope with these massive commercial projects.”

The oldest known fossils of pollen-laden insects are of earwig-like ground-dwellers that lived in what is now Russia about 280 million years ago, researchers report. Their finding pushes back the fossil record of insects transporting pollen from one plant to another, a key aspect of modern-day pollination, by about 120 million years.

The insects — from a pollen-eating genus named Tillyardembia first described in 1937 — were typically about 1.5 centimeters long, says Alexander Khramov, a paleoentomologist at the Borissiak Paleontological Institute in Moscow. Flimsy wings probably kept the creatures mostly on the forest floor, he says, leaving them to climb trees to find and consume their pollen.

Recently, Khramov and his colleagues scrutinized 425 fossils of Tillyardembia in the institute’s collection. Six had clumps of pollen grains trapped on their heads, legs, thoraxes or abdomens, the team reports February 28 in Biology Letters. A proportion that small isn’t surprising, Khramov says, because the fossils were preserved in what started out as fine-grained sediments. The early stages of fossilization in such material would tend to wash away pollen from the insects’ remains.
The pollen-laden insects had only a couple of types of pollen trapped on them, the team found, suggesting that the critters were very selective in the tree species they visited. “That sort of specialization is in line with potential pollinators,” says Michael Engel, a paleoentomologist at the University of Kansas in Lawrence who was not involved in the study. “There’s probably vast amounts of such specialization that occurred even before Tillyardembia, we just don’t have evidence of it yet.”

Further study of these fossils might reveal if Tillyardembia had evolved special pollen-trapping hairs or other such structures on their bodies or heads, says Conrad Labandeira, a paleoecologist at the National Museum of Natural History in Washington, D.C., also not part of the study. It would also be interesting, he says, to see if something about the pollen helped it stick to the insects. If the pollen grains had structures that enabled them to clump more readily, for example, then those same features may have helped them grab Velcro-like onto any hairlike structures on the insects’ bodies.

To shrink error rates in quantum computers, sometimes more is better. More qubits, that is.

The quantum bits, or qubits, that make up a quantum computer are prone to mistakes that could render a calculation useless if not corrected. To reduce that error rate, scientists aim to build a computer that can correct its own errors. Such a machine would combine the powers of multiple fallible qubits into one improved qubit, called a “logical qubit,” that can be used to make calculations (SN: 6/22/20).

Scientists now have demonstrated a key milestone in quantum error correction. Scaling up the number of qubits in a logical qubit can make it less error-prone, researchers at Google report February 22 in Nature.
Future quantum computers could solve problems impossible for even the most powerful traditional computers (SN: 6/29/17). To build those mighty quantum machines, researchers agree that they’ll need to use error correction to dramatically shrink error rates. While scientists have previously demonstrated that they can detect and correct simple errors in small-scale quantum computers, error correction is still in its early stages (SN: 10/4/21).

The new advance doesn’t mean researchers are ready to build a fully error-corrected quantum computer, “however, it does demonstrate that it is indeed possible, that error correction fundamentally works,” physicist Julian Kelly of Google Quantum AI said in a news briefing February 21.
Logical qubits store information redundantly in multiple physical qubits. That redundancy allows a quantum computer to check if any mistakes have cropped up and fix them on the fly. Ideally, the larger the logical qubit, the smaller the error rate should be. But if the original qubits are too faulty, adding in more of them will cause more problems than it solves.

Using Google’s Sycamore quantum chip, the researchers studied two different sizes of logical qubits, one consisting of 17 qubits and the other of 49 qubits. After making steady improvements to the performance of the original physical qubits that make up the device, the researchers tallied up the errors that still slipped through. The larger logical qubit had a lower error rate, about 2.9 percent per round of error correction, compared to the smaller logical qubit’s rate of about 3.0 percent, the researchers found.
That small improvement suggests scientists are finally tiptoeing into the regime where error correction can begin to squelch errors by scaling up. “It’s a major goal to achieve,” says physicist Andreas Wallraff of ETH Zurich, who was not involved with the research.

However, the result is only on the cusp of showing that error correction improves as scientists scale up. A computer simulation of the quantum computer’s performance suggests that, if the logical qubit’s size were increased even more, its error rate would actually get worse. Additional improvement to the original faulty qubits will be needed to enable scientists to really capitalize on the benefits of error correction.

Still, milestones in quantum computation are so difficult to achieve that they’re treated like pole jumping, Wallraff says. You just aim to barely clear the bar.

Fungi may help some tree-killer beetles turn a tree’s natural defense system against itself.

The Eurasian spruce bark beetle (Ips typographus) has massacred millions of conifers in forests across Europe. Now, research suggests that fungi associated with these bark beetles are key players in the insect’s hostile takeovers. These fungi warp the chemical defenses of host trees to create an aroma that attracts beetles to burrow, researchers report February 21 in PLOS Biology.

This fungi-made perfume might explain why bark beetles tend to swarm the same tree. As climate change makes Europe’s forests more vulnerable to insect invasions, understanding this relationship could help scientists develop new countermeasures to ward off beetle attacks.
Bark beetles are a type of insect found around the world that feed and breed inside trees (SN: 12/17/10). In recent years, several bark beetle species have aggressively attacked forests from North America to Australia, leaving ominous strands of dead trees in their wake.

But trees aren’t defenseless. Conifers — which include pine and fir trees — are veritable chemical weapons factories. The evergreen smell of Christmas trees and alpine forests comes from airborne varieties of these chemicals. But while they may smell delightful, these chemicals’ main purpose is to trap and poison invaders.

Or at least, that’s what they’re meant to do.

“Conifers are full of resin and other stuff that should do horrible things to insects,” says Jonathan Gershenzon, a chemical ecologist at the Max Planck Institute for Chemical Ecology in Jena, Germany. “But bark beetles don’t seem to mind at all.”

This ability of bark beetles to overcome the powerful defense system of conifers has led some scientists to wonder if fungi might be helping. Fungi break down compounds in their environment for food and protection (SN: 11/30/21). And some type of fungi — including some species in the genus Grosmannia — are always found in association with Eurasian spruce bark beetles.
Gershenzon and his colleagues compared the chemicals released by spruce bark infested with Grosmannia and other fungi to the chemical profile of uninfected trees. The presence of the fungi fundamentally changed the chemical profile of spruce trees, the team found. More than half the airborne chemicals — made by fungi breaking down monoterpenes and other chemicals that are likely part of the tree defense system — were unique to infected trees after 12 days.

This is surprising because researchers had previously assumed that invading fungi hardly changed the chemical profile of trees, says Jonathan Cale, a fungal ecologist at the University of Northern British Columbia in Prince George, Canada, who was not involved with the research.
Later experiments revealed that bark beetles can detect many of these fungi-made chemicals. The team tested this by attaching tiny electrodes on bark beetles’ heads and detecting electrical activity when the chemicals wafted passed their antennae. What’s more, the smell of these chemicals combined with beetle pheromones led the insects to burrow at higher rates than the smell of pheromones alone.

The study suggests that these fungi-made chemicals can help beetles tell where to feed and breed, possibly by advertising that the fungi has taken down some of the tree’s defenses. The attractive nature of the chemicals could also explain the beetle’s swarming behavior, which drives the death of healthy adult trees.

But while the fungi aroma might doom trees, it could also lead to the beetles’ demise. Beetle traps in Europe currently use only beetle pheromones to attract their victims. Combining pheromones with fungi-derived chemicals might be the secret to entice more beetles into traps, making them more effective.

The results present “an exciting direction for developing new tools to manage destructive bark beetle outbreaks” for other beetle species as well, Cale says. In North America, mild winters and drought have put conifer forests at greater risk from mountain pine beetle (Dendroctonus pendersoae) attacks. Finding and using fungi-derived chemicals might be one way to fend off the worst of the bark beetle invasions in years to come.